维敏四联治疗Hp相关的消化性溃疡

目的应用维敏胶囊（胶态果胶铋）四联药物疗法治疗Hp相关的消化性溃疡（PU）2wk，停药4wk后经内镜、14C-UBT等方法观察溃疡的愈合及Hp根除的疗效方法经内镜确诊为PU，其中十二指肠溃疡（DU）169例；胃溃疡（GU）89例．受检前2wk内未服抗生素、铋剂及质子泵阻断剂，排除孕妇和溃疡出血者，并镜下活检病理排除恶性溃疡Hp检测：先行快速尿素酶检测（RUT），阳性者再行14C-UBT检测，其中DU的Hp阳性率为95．5％；GU的Hp阳性率为81．0％．四联治疗方法：对Hp阳性PU，给予维敏胶囊100mg，4次／d；兰索拉唑30mg，2次／d；阿莫西林0．5g，4次／d；甲硝唑0．4g，2次／d，疗程为2wk．停药后4wk，同时复查内镜及14G-UBT．结果DU愈合率91．2％，Hp根除率93．0％；GU愈合率86．0％，Hp根除率92．0％．DU和GU愈合率及Hp根除率差异不明显（P＞0．05）；四联疗法后肝肾功能无异常结论Hp与PU关系密切．采用四联治疗Hp相关的PU，有良好效果．14GUBT检测Hp感染具有很高的敏感性和特异性，无创伤性，是治疗后复查Hp的首选方法     

食管静脉曲张结扎术后门脉高压性胃病加重的相关因素分析

目的分析食管静脉曲张结扎术（EVL）后导致门脉高压性胃病（PHG）加重的各种相关危险因素。方法回顾性分析154例肝硬化患者施行EVL前后PHG的加重程度。结果43例有门奇静脉断流术史伴H．pylori阳性者,EVL前后患者重度PHG的总构成比分别为51．16％和74．42％（P〈0．05）;按肝功能Child—Pugh（A＋B）级、C级分组,各组患者EVL前后的重度PHG构成比分别为30．77％、38．46％（P〉0．05）和60．00％、90．00％（P〈0．05）。33例有门奇静脉断流术史H．pylori阴性者,EVL前后的重度PHG总构成比分别为21．21％和36．36％（P〈0．05）。按肝功能Child—Pugh（A＋B）级、C级分组,各组患者EVL前后的重度PHG总构成比为14．29％、21．43％（P〉0．05）和26．32％、47．37％（P〈0．05）。15例无门奇脉断流术史H．pylori阳性者,EVL前后的重度PHG的总构成比分别为20．00％和40．00％（P〈0．05）;按肝功能Child—Pugh（A＋B）级、c级分组,各组患者EVL前后的重度PHG构成比分别为16．67％、16．67％（P〈0．01）和22．22％（1／6）、55．56％（P〈0．01）。46例无门奇脉断流术史鼠pylori阴性者,EVL前后重度PHG的总构成比分别为17．39％和23．91％（P〉0．05）;按肝功能Child—Pugh（A＋B）级和c级分组,各组患者EVL前后的重度PHG构成比分别为14．29％、19．05％（P〉0．05）和20．00％、28．00％（P〈0．05）。结论肝硬化患者EVL前后的重度PHG构成比率与肝功能Child—Pugh分级呈明显正相关;门奇静脉断流术、H．pylori感染均为肝硬化患者EVL后引起PHG程度加重的重要危险因素。     

胃及十二指肠球部溃疡的内镜调查报告

目的利用内镜资料调查胃溃疡（GU）和十二指肠球部溃疡（DU）的某些临床流行病学特点．方法收集5a的内镜资料，统计GU，DU的检出率及发病季节，性别及年龄分布等特点及幽门螺杆菌的检出情况．结果5405例受检病例中共检出DU1236例，GU197例，检出率分别为22．9％和3．6％．DU检出率以1月～3月份及12月份最高（27．7％～32．0％，平均30．2％），6月～8月份最低（16．1％～16．8％，平均17．2％，与1月～3月份及12月份平均检出率比较，P＜0．01）．GU的检出率无明显季节差异（P＞0．05）．DU，GU的男女之比分别为5．43：1和3．40：1，男女性检出率分别为26．8％和12．7％（P＜0．01），3．9％和3．0％（P＞0．05）．40岁以上者GU检出率为6．5％（其中60岁以上者为9．1％），40岁以下者为2．6％（与40岁以上者比较，P＜0．01），而DU的检出率无明显年龄差异．214例溃疡患者胃粘膜尿素酶试验阳性率为76．6％，其中DU为77．6％，GU为72．5％．结论DU的发病与季节气候有关，冬春季较夏秋季更易发病；GU发病与季节无关．DU和GU均以男性多发，其检出率男性明显高于女性．GU多见于40岁以上患者，而且年龄愈大检出率愈高；DU的检出率无年龄差异．     

幽门螺杆菌相关性消化性溃疡的细胞凋亡研究

目的：探讨幽门螺杆菌（Helicobacter pylori,HP)诱导胃上皮细胞凋亡的机制及细胞凋亡在HP相关性消化性溃疡（PU）中的作用。方法：内镜下胃粘膜活检取材,应用TUNEL法检测胃上皮细胞凋亡,免疫组化法检测凋亡调控蛋白bak、bcl-2的表达。结果：HP阳性胃溃疡（GU）和十二指肠（DU）患者细胞凋亡指数（AI）明显高于HP阴性非溃疡性消化不良（NUD）患者（P＜0．01）。根除HP后,AI在DU明显下降（P＜0．01）,在GU无明显改变（P＞0．05）。HP阳性DU溃疡活动期AI明显高于愈合期和瘢痕期（P＜0．05）,而HP阳性和GU溃疡三期AI无差异（P＞0．05）。bak蛋白表达在HP阳性PU明显高于HP阴性NUD患者（P＜0．05）。根除HP后,DU患者bak蛋白表达明显降低（P＜0．05）。GU患者虽有下降,但无统计学差异。bcl-2蛋白表达在HP阳性PU与HP阴性NUD之间无显著差异,HP根除前后亦无明显改变。结论：HP诱导胃上皮细胞凋亡在十二指肠溃疡发病中起重要的作用,HP诱导胃上皮细胞凋亡可能是通过bak路径实现的。     

胃石并发溃疡与幽门螺杆菌的关系探讨

目的探讨胃石溃疡并发症的发生及其愈合与幽门螺杆菌（Hp）的关系。方法对内镜下发现的93例胃石症患者均钳取胃黏膜标本,并采取快速尿素酶试验及^14C呼气试验检测Hp感染;清除胃石并经过4周的常规抑酸及保护胃黏膜治疗,分别于治疗2周、4周后复查胃镜观察溃疡愈合情况。结果93例胃石患者中,Hp检测阳性57例、阴性36例;胃石合并溃疡与无溃疡并发症者Hp感染率分别为64．58％、57．78％（P〉0．05）;治疗2周后,有Hp感染和无Hp感染患者愈合率分别为30％、68．75％（P〈0．05）,4周后分别为96．67％、100％（P〉0．05）。结论胃石溃疡并发症的发生可能与Hp感染无明显关系,但Hp感染可能影响其溃疡并发症的愈合。     

cag A阳性幽门螺杆菌与老年胃十二指肠病的相关性

目的 探讨本地区老人幽门螺杆菌（Hp）tagA基因存在状况及其与老年胃十二指肠病的关系。方法 收集89例老年和96例青壮年慢性胃炎、消化性溃疡患菌及30例正常对照人群的血清标本及胃组织标本,应用血清学检验其Hp-cag A阳性菌株感染状况。结果 89例老年患者中慢性胃炎、胃溃疡、十二指肠溃疡的Hp-cag A基因的阳性率分别为73．5％（38／52）、81．3％（13／16）及85．7％（18／21）;96例青壮年患者中慢性胃炎、胃溃疡、十二指肠溃疡的Hp-cag A基因的阳性率分别为59．3％（32／54）、68．8％（11／16）及61．5％（16／26）;对照组Hp-cag A阳性病株感染率为33．3％,各疾病组间Hp-cag A阳件菌株感染率差异无显著性（P〉0．05）．仍均高于对照组（P〈0．05）;cag A阳性Hp菌株感染率老年组高于青壮年组（P〈0．05）。结论 本地区老年患者cag A阳性Hp菌株感染与上述3种胃十二指肠疚病的发生均密切相关．老年患者感染的Hp绝大多数为cag A阳性菌株。     

崇信县城乡Hp感染特点

目的城乡幽门螺杆菌（Hp）感染与胃炎、消化性溃疡、胃癌的特点．方法城乡Hp感染阳性患者403例，城市62例、农村341例，以内镜检查次数分别统计胃炎（CG）、胃溃疡（GU），十二指肠溃疡（DU）、胃癌（GC）、Hp阳性例数，并对年龄性别，城乡进行登记．应用珠海克隆科技公司生产的Hp检测试纸，在内镜下用普通活检钳取胃窦，体粘膜及病变活体组织，涂入该试纸上，试纸颜色由黄色变为红色Hp（＋），不变色为阴性．5a内镜检查数和消化性溃疡、胃炎、胃癌检出数及城乡两级分表统计．结果403例Hp阳性患者年龄22岁～76岁，平均年龄35．87岁，城市35．20岁，农村36．84岁．CG平均年龄35．20岁，城市34.30岁，农村38．84岁．GU平均年龄36.43岁，城市34．86岁，农村37．65岁．DU平均年龄37．25岁，城市35．78岁，农村37.48岁．GC平均年龄37．25岁，城市39．28岁，农村41．10岁．403例Hp阳性患者城市检出率15．4％，农村Hp阳性检出率84．6％．农村检出率显著高于城市经统计学处理有显著差异（P＜0．01）．结论总Hp感染率71．33％，复合流行病学调查我国人群Hp感染率在50％～80％之间．性别无明显差异．     

老年人消化性溃疡与却感染、服用非甾体消炎药的关系

目的 探讨老年人消化性溃疡（PU）及其常见并发症出血与幽门螺杆菌（Hp）感染、服用非甾体消炎药（NSAIDs）之间的关系。方法 采用病例对照分析方法，收集60岁以上老年消化性溃疡病（PUD）连续住院患者784例为研究组．再根据有无并发出血将研究组分为出血亚组（416例）与非出血亚组（368例）：选同期住院的60岁及以上老年慢性胃炎患者261例为对照组．所有患者均经胃镜明确诊断．并进行Hp快速尿素酶试验．统计患者NSAIDs的服用情况。结果 ①研究组服用NSAIDs的百分率及坳感染率均显著高于对照组（P〈0．05）；②研究组出血亚组服NSAIDs者的Hp阳性率（22．6％）低于未服NSAIDs者（73．8％）（P〈0．05）；③非出血亚组服NSAIDs者的Hp阳性率（30．0％）低于未服NSAIDs者（82．0％）（P〈0．05）；④研究组出血亚组中无论胃溃疡（Gu）还是十二指肠溃疡（Du）患者服用NSAIDs百分率均高于非出血亚组（P〈0．05）；出血亚组中GU患者却感染率（62％）比非出血组（82．5％）明显降低（P〈0．05），而出血亚组中DU患者Hp感染率（66．7％）与非出血组（70．6％）比较无明显差别（P〉0．05）。结论 ①老年人PUD的发病与Hp感染及服用NSAIDs密切相关，②服用NSAIDs可以增加老年PUD出血的危险性，而Hp感染并不增加老年PUD出血的危险性。③老年人PUD（不论出血和非出血）服NSAIDs者坳感染率降低。     

上海地区幽门螺杆菌菌株iceA、babA2基因型与临床的关系

目的检测上海地区幽门螺杆菌(Hp)感染患者中Hp菌株iceA、babA2的分布特征，探讨与Hp临床感染结局相关的菌株基因型。方法141株Hp菌株分离自43例慢性胃炎(CG)、47例十二指肠球部溃疡(DU)、30例胃溃疡(GU)和21例非贲门部胃癌患者的胃镜活检标本。采用PCR方法检测Hp菌株的iceA、babA2、cagA和vacA基因型。结果141株Hp菌株中，iceA1、iceA2和babA2的总检出率分别为74．5％(105／141)、15．6％(22／141)和63．8％(90／141)，其中2例(1．4％)为iceA1、iceA2均阳性，16例(11．3％)为iceA1、iceA2均阴性。DU组的babA2检出率显著高于GU组(74．5％比50．0％。P=0．028)，DU组的cagA^ ／babA2^ 检出率亦显著高于GU组(70．2％比46．7％，P=0．039)。其余疾病组之间的babA2检出率差异无显著性。未发现不同临床疾病与iceA基因型的相关性。结论上海地区Hp感染者的菌株基因型主要是iceA1^ ／babA2^ ，babA2在DU和GU的发病机制中起不同作用。未发现iceA亚型与Hp临床感染结局有相关性。     

幽门螺杆菌感染与胃、十二指肠疾病相关性探析

目的对有上消化道症状而作内镜检查的患者进行幽门螺杆菌（Hp）检测，以了解云南江川地区Hp感染与胃、十二指肠炎、溃疡及胃癌疾病发生的相关性．方法在内镜直视下取材，慢性胃炎、十二指肠溃疡在胃窦部大弯侧幽门前1cm～3cm，胃溃疡、胃癌分别在溃疡及癌肿边缘取材标本1～2块．将活检取材标本置入福建三强生物化工有限公司生产的Hp感染快速诊断试剂盒（HpVT，SQ-H102）孔内，阳性病例5min内呈红色，简称（尿素酶试验）．结果1022例中，Hp阳性者639例，占62．5％，其中慢性浅表性胃炎（CSG）66．5％（381／573）；慢性萎缩性胃炎（CAG）26％（18／69）；胃溃疡（GU）51．9％（42／81）；十二指肠溃疡（DU）68．4％（195／285）；胃癌（GCa）33．3％．（3／9）．病种不同，Hp阳性率亦略有差异．不同年龄组Hp阳性率经统计学处理无明显差异（P＜0．05）．结论本组与国内其他报道相比较要比他们的阳性率低，可能与云贵高原气候；人群居住分散；人们常年吃生大蒜等因素有关．亦可能与本组仅作尿素酶检查有关要提高Hp感染阳性率的检测水平，现急需有简便、敏感性强，价廉的检测方法，在基层医院推广应用．     

Changing trends in peptic ulcer prevalence in a tertiary care setting in the Philippines: a seven-year study

BACKGROUND AND AIMS: The declining global prevalence of peptic ulcer disease (PUD) might be because of the decreasing prevalence of Helicobacter pylori (Hp) infection. The aims of the present study were to determine the prevalence of PUD during a 7-year period and to investigate its relationship with the prevalence of Hp infection during the same period. METHODS: All upper gastrointestinal endoscopies carried out at Santo Tomas Hospital in Manila from January 1996 to December 2002 were evaluated. Endoscopies reporting gastric ulcers (GU) and duodenal ulcers (DU) with Hp status were analyzed. RESULTS: A total of 15 341 endoscopies were evaluated. Overall, 2600 (16.95%) GU and 1575 (10.27%) DU were identified. There was a decreasing trend in the prevalence of GU (P < 0.0001) and DU (P < 0.0001) during the study period. Overall PUD prevalence declined from 35.87% in 1996 to 18.80% in 2002. This decline was seen for both GU and DU (20.05 vs 14.34%, and 15.83 vs 7.02%, respectively). The prevalence of Hp infection decreased significantly from 1996 to 2002 for both GU and DU (68.13 vs 33.48%, P < 0.0001; and 76.67 vs 36.50%, P < 0.0001, respectively). The decrease in Hp prevalence was significantly related to the decrease in ulcer prevalence (r = 0.97, P = 0.0004 for GU; r = 0.89, P = 0.0079 for DU; and r = 0.92, P = 0.0035 for all PUD). The prevalence of bleeding secondary to PUD remained stable during the 7-year period (P = 0.87). CONCLUSIONS: During the 7-year period, there was a significant decline in the prevalence of PUD. This decline in PUD prevalence was associated with a corresponding decrease in Hp prevalence.     

Clinical relevance of Helicobacter pylori CagA-positive strains: gastroduodenal peptic lesions marker.

OBJECTIVES: peptic ulcer is characterized by its recurrent nature, which necessitates maintenance treatment in most patients. But this natural history can be changed in patients with peptic ulcer associated to Helicobacter pylori, as shown by the low rates of recurrence and decreased hemorrhagic recidivism associated with this infection. Whether CagA or VacA strains are associated with a greater risk of peptic ulcer is controversial. This study was designed to examine endoscopic findings and their relation with H. pylori phenotype (CagA or VacA). METHODS: 106 selected dyspeptic patients underwent upper gastrointestinal tract endoscopic examination between September 1996 and May 1997 [69 with H. pylori (Hp) and 37 without this infection]. Endoscopic findings were classified as gastric ulcer (GU), duodenal ulcer (DU), gastric erosions (GE), duodenitis (Du), chronic gastritis (CG) and normal mucosa (NM). Hp phenotype was analyzed with a western blot test. RESULTS: 75% of H. pylori strains were CagA-positive and 54.2% were VacA-positive. 82.4% of the cases of DU were associated with a CagA+ phenotype, but the association was not statistically significant. Otherwise 100% of gastric ulcers were associated with CagA+ strains (p < 0.005). VacA phenotype was not associated with any particular endoscopic finding. Peptic ulcer (DU or GU) was also associated with the CagA+ phenotype (p < 0.05). CONCLUSIONS: the CagA+ H. pylori phenotype seems to be a peptic lesion marker, but was more frequently related with GU than with DU in our sample of Spanish patients.     

肝硬化上消化道出血和幽门螺杆菌感染的相关性研究

目的研究肝硬化患者幽门螺杆菌感染和上消化道出血之间的关系.方法肝硬化患者160例,内镜检查了解食管静脉曲张和消化性溃疡的发生情况及出血的原因,同时胃粘膜活检作尿素酶试验,检测幽门螺杆菌(Hp).结果Hp阳性组消化性溃疡发生率(64.1%)明显高于阴性组(37.8%,P＜0.01).出血率在Hp阳性组(38.5%)也明显高于阴性组(22%,P＜0.05).结论Hp感染和肝源性溃疡发生有关,Hp感染者的肝源性溃疡发生率增高及胃粘膜活动性炎症可能导致出血率升高,根除Hp有可能降低肝硬化上消化道出血.     

Prevalence and genetic diversity of cagD, cagE, and vacA in Helicobacter pylori strains isolated from Japanese patients

BACKGROUND: Although cagD and cagE (cagDE) identified upstream of cagA have been shown to be involved in the induction of interleukin (IL)-8 expression, the relationship between cagDE status and gastroduodenal diseases still remains to be examined. Thus we investigated prevalence and genetic diversity of cagD, cagE, and vacA in Helicobacter pylori strains isolated from patients with peptic ulcer or gastritis. METHODS: We analyzed 73 H. pylori strains isolated from Japanese patients (gastritis (GA), 15; gastric ulcer (GU), 28; duodenal ulcer (DU), 23; GU and DU, 7). The presence of cagDE was evaluated by polymerase chain reaction (PCR) and Southern hybridization. The vacA genotype was examined by PCR, using type-specific primers. RESULTS: cagDE was present in 13 (86.7%) of 15 patients with GA, 26 (92.9%) of 28 patients with GU, 21 (91.3%) of 23 patients with DU, and 6 (85.7%) of 7 patients with GU and DU (P = 0.89). vacA signal sequence type s1 was found in 14 (93.3%) of 15 patients with GA, 26 (92.9%) of 28 patients with GU, 22 (95.7%) of 23 patients with DU, and 6 (85.7%) of 7 patients with GU and DU (P = 0.84). Sequences of cagDE and vacA in our Japanese strains were highly homologous with one another, and there were no disease-specific mutations. CONCLUSIONS: Most of the H. pylori strains in Japan were cagDE-positive, vacA s1 type, regardless of clinical outcome. The present study also indicated that these genes were conserved well among our H. pylori isolates.     

High Prevalence of Helicobacter pylori in Liver Cirrhosis (Relationship with Clinical and Endoscopic Features and the Risk of Peptic Ulcer)

In 153 consecutive patients with cirrhosis weassessed: (1) the prevalence of IgG to Helicobacterpylori and compared it with that found in 1010 blooddonors resident in the same area; and (2) therelationships of IgG to Helicobacter pylori with clinical andendoscopic features and with the risk of peptic ulcer.The IgG to Helicobacter pylori prevalence of cirrhoticswas significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was notassociated with sex, cirrhosis etiology, Child class,gammaglobulins and hypertensive gastropathy. In bothgroups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Amongpatients with cirrhosis a significantly higherprevalence of Helicobacter pylori was found in patientswith previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) andpatients with peptic ulcer (P = 0.0004). Multivariateanalysis identified increasing age and male sex as riskfactors for a positive Helicobacter pylori serology and no independent risk factors for pepticulcer. The high prevalence of Helicobacterpylori-positive serology found in the present series isrelated to age and sex and might also be explained byprevious hospital admissions and/or uppergastrointestinal endoscopy. Our results do not confirmthe role of Helicobacter pylori as risk factor forpeptic ulcer in patients with liver cirrhosis.     

Hp相关性胃疾病与胃肠化生、不典型增生的关系

目的探讨Hp感染与肠化生、不典型增生等胃癌前期病变的关系.方法693例胃病患者,分慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、胃溃疡(GU)及十二指球部溃疡(DU)等四组,胃镜下观察粘膜病变、溃疡部位及性质,胃镜下取材,常规HE染色后观察组织学改变、Giemsa染色后观察Hp感染程度,统计分析Hp感染与肠化生、不典型增生等的关系.结果四组胃疾病中,Hp感染程度与肠化尘程度差异显著(P＜0.01),DU组的Hp感染率高于其它组(P＜0.01),CAG组的胃肠化生率最高(P＜0.05);Hp阳性标本中,CAG组的胃肠化及不典型增生最高(P＜0.01)Hp阴性标本中,CAG组的胃肠本的胃肠化和不典型增生发生率与Hp阴性标本的发生率有显著差异(P＜0.05).结论Hp与CAG并存时,癌前病变发生率最高,其次为GU;建议在临床上,抗Hp治疗和对CAG、GU的治疗同时进行,并内镜随访.     

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.     

Gastric Carcinoid Tumors Without Autoimmune Gastritis in Japan: A Relationship with Helicobacter pylori Infection

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.